Document 0175
 DOCN  M95A0175
 TI    Lentiviral infection, immune response peptides and sleep.
 DT    9510
 AU    Darko DF; Mitler MM; Henriksen SJ; Scripps Research Institute, La Jolla,
       CA 92037-1027, USA.
 SO    Adv Neuroimmunol. 1995;5(1):57-77. Unique Identifier : AIDSLINE
       MED/95316270
 AB    The aberrant sleep documented in subjects with human immunodeficiency
       virus (HIV) infection is uniquely important because of the contribution
       this poor quality sleep makes to the fatigue, disability, and eventual
       unemployment that befalls these patients. Especially given this
       importance in clinical care, the research on the prominent sleep changes
       described in HIV infection remains modest in quantity. The chronic
       asymptomatic stage of HIV infection is associated with the most
       intriguing and singular sleep structure changes. Especially robust is
       the increase in slow wave sleep, particularly in latter portions of the
       sleep period. This finding is rare in other primary or secondary sleep
       disorders. The sleep structure alterations are among the most replicable
       of several pathophysiological sequelae in the brain associated with
       early HIV infection. It is unlikely that these sleep architecture
       changes are psychosocial in etiology, and they occur before medical
       pathology is evident. They are not associated with stress, anxiety, or
       depression. Evidence is accumulating to support a role for the
       somnogenic immune peptides tumor necrosis factor (TNF)alpha and
       interleukin (IL-1 beta) in the sleep changes and fatigue commonly seen
       in HIV infection. These peptides are elevated in the blood of
       HIV-infected individuals, and are somnogenic in clinical use and animal
       models. The peripheral production of these peptides may also have a role
       in the regulation of normal sleep physiology. The lentivirus family
       contains both HIV and the feline immunodeficiency virus (FIV). The use
       of the FIV model of HIV infection may provide a way to further
       investigate the mechanism of a neurotropic, neurotoxic virus initiating
       the immune acute phase response and affecting sleep. Neurotropic
       lentivirus infection is a microbiological probe facilitating neuroimmune
       investigation.
 DE    Acute Disease  Animal  AIDS Dementia Complex/ETIOLOGY  Cats  Chronic
       Disease  Fatigue/ETIOLOGY  Feline Acquired Immunodeficiency
       Syndrome/COMPLICATIONS/  IMMUNOLOGY  Human  HIV
       Infections/*COMPLICATIONS/IMMUNOLOGY  Interleukin-1/*PHYSIOLOGY  Male
       Models, Neurological  Neuroimmunomodulation/*PHYSIOLOGY  Polysomnography
       Sleep Disorders/*ETIOLOGY/IMMUNOLOGY  Sleep Stages/PHYSIOLOGY  Support,
       U.S. Gov't, P.H.S.  Tumor Necrosis Factor/*PHYSIOLOGY  JOURNAL ARTICLE
       REVIEW  REVIEW, ACADEMIC

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).